TY - JOUR
T1 - A delayed increase in hippocampal proliferation following global asphyxia in the neonatal rat
AU - Scheepens, Arjan
AU - Wassink, Guido
AU - Piersma, Marrit J
AU - Van de Berg, Wilma D J
AU - Blanco, Carlos E
PY - 2003/4/14
Y1 - 2003/4/14
N2 - Adult neurogenesis has been shown to be upregulated following a wide variety of brain injury paradigms. During the first weeks of postnatal life there is around 50 fold more neurogenesis occurring than in the adult CNS, yet little is known regarding the effect of neonatal brain injury on this developmental proliferation. We have investigated the effect of a global perinatal birth asphyxia on postnatal proliferation at 2, 5, 8, 11, 15, 21 and 28 days after birth (injury) using a 3H-thymidine tracer study. We found a specific upregulation of proliferation at 5 days after the injury within the injured hippocampus only, with an associated increase in hippocampal mass and without any changes in GFAP content at any timepoint. Perinatal asphyxia did not alter proliferation within the cerebellum, sub ventricular zone, olfactory bulb, cervical or thoracic spinal cord. Similarly, no changes in corticosterone levels were induced by the injury. Since there were no changes in GFAP content we hypothesize that this increased proliferation is likely neurogenetic, similar to what is seen in the adult brain following injury. Further we show that the dramatic increase in corticosterone at the end of the stress hyporesponsive period is not responsible for the equally dramatic decrease in postnatal proliferation within the CNS.
AB - Adult neurogenesis has been shown to be upregulated following a wide variety of brain injury paradigms. During the first weeks of postnatal life there is around 50 fold more neurogenesis occurring than in the adult CNS, yet little is known regarding the effect of neonatal brain injury on this developmental proliferation. We have investigated the effect of a global perinatal birth asphyxia on postnatal proliferation at 2, 5, 8, 11, 15, 21 and 28 days after birth (injury) using a 3H-thymidine tracer study. We found a specific upregulation of proliferation at 5 days after the injury within the injured hippocampus only, with an associated increase in hippocampal mass and without any changes in GFAP content at any timepoint. Perinatal asphyxia did not alter proliferation within the cerebellum, sub ventricular zone, olfactory bulb, cervical or thoracic spinal cord. Similarly, no changes in corticosterone levels were induced by the injury. Since there were no changes in GFAP content we hypothesize that this increased proliferation is likely neurogenetic, similar to what is seen in the adult brain following injury. Further we show that the dramatic increase in corticosterone at the end of the stress hyporesponsive period is not responsible for the equally dramatic decrease in postnatal proliferation within the CNS.
KW - Animals
KW - Animals, Newborn
KW - Cell Division/physiology
KW - Central Nervous System/growth & development
KW - Corticosterone/blood
KW - Enzyme-Linked Immunosorbent Assay
KW - Female
KW - Glial Fibrillary Acidic Protein/metabolism
KW - Hippocampus/growth & development
KW - Hypoxia, Brain/blood
KW - Male
KW - Pregnancy
KW - Rats
KW - Rats, Wistar
M3 - Article
C2 - 12694945
VL - 142
SP - 67
EP - 76
JO - DEVELOPMENTAL BRAIN RESEARCH
JF - DEVELOPMENTAL BRAIN RESEARCH
SN - 0165-3806
IS - 1
ER -